Psychosis in A Patient With Silent Vascular Brain Lesions

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Psychosis in a Patient With Silent Vascular Brain Lesions

Article  in  The Journal of Neuropsychiatry and Clinical Neurosciences · December 2012


DOI: 10.1176/appi.neuropsych.11010030 · Source: PubMed

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LETTERS

Psychosis in a Patient With years ago, whereas the depressive was diagnosed with Vascular
Silent Vascular Brain Lesions symptoms had been present for the Dementia with Delusions and
past 3 months. The patient scored Depressed Mood, and Alcohol
18/30 on the Montreal Cognitive Dependence, according to DSM-
Assessment, with impairment in IV-TR criteria. During his present
To the Editor: A plethora of infor- visuospatial/executive skills, atten- admission, the patient was treated
mation is available on psychiatric tion, verbal fluency, and delayed with sertraline (150 mg/day) and
disorders after vascular brain recall.3 He scored 11/18 on the quetiapine (100 mg/day), with
lesions presenting clinically as Frontal Assessment Battery, with improvement in both depressive
stroke, but there is scant literature impairment in conceptualization, and psychotic symptoms. He did
on silent vascular brain lesions or lexical fluency, programming, and not consent to a trial of donepezil.
infarcts without any overt neuro- inhibitory (Go/No-Go) domains.4
logical signs or symptoms present- His blood counts, electrolytes, renal Discussion
ing with psychiatric disorders. The function tests, TSH, B12, and folic A silent cerebral infarction can
extant literature on silent brain acid were normal. Urine analysis present with one of the four psy-
infarctions has focused mainly on and urine drug screen were non- chiatric symptom clusters: affective,
depression and, to some extent, on contributory. Neurologic examina- paranoid delusional, confusional
mania, while psychosis in this tion was unremarkable. Abnormal state, and changes in mood with
context has only been rarely laboratory parameters included behavioral disturbance.5 However,
described.1,2 We describe a case of fasting glucose (128 mg/dl), ala- without a high index of suspicion,
psychosis in a patient with silent nine aminotransferase (82 units/ these silent vascular brain lesions
vascular lesions in the right frontal liter), and aspartate aminotransfer- are like1y to be missed in patients
lobe and discuss the interplay of ase (81 units/liter). Head CT scan presenting with prototypical psy-
cognitive deficits and psychiatric showed an area of encephalomala- chiatric syndromes. In our patient,
presentation in such cases. cia (1.3 cm x 2.2 cm) in the anterior besides the vascular brain changes,
and lateral aspect of the right fron- chronic alcohol use, comorbid
Case Report tal lobe. There were scattered low- depression, and, possibly, vascular
A 69-year-old white man was attenuation foci in the external cap- dementia itself may have contrib-
transferred from the intensive care sule bilaterally, left more than uted to the presentation. Right-side
unit, where he was being treated right. The head CT results did not brain lesions are more common in
for possible delirium tremens, to differ from another study done patients who develop psychosis
the psychiatric unit, for persistent about 3 years ago (done after after stroke.6 –8 The role of frontal
depressive and psychotic symp- the patient had a fall), but neither lobe deficits in this patient also
toms. He had a longstanding his- the patient nor his family were deserves mention. Delusions in
tory of alcohol use. He also had aware of the results of the previous patients with dementia are associ-
type 2 diabetes mellitus, dyslipide- head CT. However, the family did ated with frontal lobe changes,9
mia, and coronary artery disease, corroborate the onset of the and patients with psychotic depres-
and had an implantable cardio- patient’s psychotic symptoms sion demonstrate fronto-temporal
verter defibrillator. During his approximately to the time of the atrophy and also do poorly on
index presentation, the patient first head CT study. Although the frontal-lobe tests, as compared with
endorsed delusions that his wife patient was started on quetiapine nonpsychotic patients.10 Thus, clini-
was having an affair with a neigh- for psychotic symptoms at that cians should explore for underlying
bor and had persecutory delusions time, the late-onset psychotic silent vascular brain lesions, espe-
regarding this person. His depres- symptoms were not correlated with cially in older patients with psy-
sive symptoms included sad mood, the head CT findings. The patient chosis and frontal lobe/executive
loss of interest, easy fatigability, and his family denied that the function deficits. Whereas vascular
trouble staying asleep, and patient was ever treated for stroke depression and mania have opera-
decreased energy. The psychotic or had any overt neurological tional definitions, more research is
symptoms had started about 3 symptoms in the past. The patient needed on “vascular psychosis” in

E20 http://neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 24:1, Winter 2012


LETTERS

this respect.11,12 It would be inter- patients with major depression. Stroke stroke. J Neuropsychiatry Clin Neurosci
esting to elucidate whether vascu- 1993; 24:1631–1634 1991; 3:6 –9
2. Fujikawa T, Yamawaki S, Touhouda Y: 9. Binetti G, Padovani A, Magni E, et al:
lar psychosis is an independent
Silent cerebral infarctions in patients Delusions and dementia: clinical and CT
entity or exists on a continuum with late-onset mania. Stroke 1995; correlates. Acta Neurol Scand 1995;
comprising vascular depression 26:946 –949 91:271–275
and vascular dementia, considering 3. Nasreddine ZS, Phillips NA, Bédirian V, 10. Simpson S, Baldwin RC, Jackson A, et al:
a report of the progression of vas- et al: The Montreal Cognitive Assess- The differentiation of DSM-III-R psy-
cular depression to vascular ment (MoCA): a brief screening tool for chotic depression in later life from non-
dementia in a patient with silent mild cognitive impairment J Am Geriatr psychotic depression: comparisons of
Soc 2005; 53:695– 699 brain changes measured by multispectral
vascular brain lesions.13
4. Dubois B, Slachesvsky A, Litvan I, et al: analysis of magnetic resonance brain
Harpreet S. Duggal, M.D. The FAB: a frontal assessment battery at images, neuropsychological findings, and
Ira Singh, M.D., M.P.H. bedside. Neurology 2000; 55:1621–1626 clinical features. Biol Psychiatry 1999;
Mental Health Branch 5. Nagaratnam N, Pathma-Nathan N: 45:193–204
Humboldt County Dept. of Behavioral and psychiatric aspects of 11. Alexopoulos GS, Meyers BS, Young
Health and Human Services silent cerebral infarction. Br J Clin Pract RC, et al: ‘Vascular depression’ hypoth-
Eureka, CA 1997; 51:160 –163 esis. Arch Gen Psychiatry 1997; 54:915–
United Indian Health Services 6. Berthier M, Starkstein S: Acute atypical 922
psychosis following a right-hemisphere 12. Wijeratne C, Malhi GS: Vascular mania:
Arcata, CA
stroke. Acta Neurol Belg 1987; 87:125– an old concept in danger of sclerosing? a
Correspondence: 131 clinical overview. Acta Psychiatr Scand
[email protected] 7. Price BH, Mesulam M: Psychiatric mani- 2007; 116(suppl. 434):35– 40
festations of right-hemisphere infarctions. 13. Loganathan S, Phutane VH, Prakash O,
J Nerv Ment Dis 1985; 173:610 – 614 et al: Psychosis in a patient with silent
References
8. Rabins PV, Starkstein SE, Robinson RG: vascular brain lesions. J Neuropsychia-
1. Fujikawa T, Yamawaki S, Touhouda Y: Risk factors for developing atypical try Clin Neurosci 2010; 22:451 e34 –
Incidence of silent cerebral infarction in (schizophreniform) psychosis following e35

J Neuropsychiatry Clin Neurosci 24:1, Winter 2012 http://neuro.psychiatryonline.org E21

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